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Some website and magazine editors have asked for a treatment of orthopedic and non-orthopedic spinal disorders, specifically the syndrome (meaning a collection of symptoms) called cauda equina or CES. While not all involve bones and articulating joints directly, there are several problems that yield symptoms that could be mistaken for those of HD (or other disorders that produce lameness) and the miscellaneous vertebral malformations that compress the spinal cord. Several, including dural ossification, are mentioned in the chapter on spinal disorders in my up-coming book on canine orthopedic disorders. Three are discussed in this article, although CES might actually comprise several disorders instead of just one.
TRANSITIONAL VERTEBRAE, TVS There has been a flurry of questions in recent years about conditions known as TVS and APA (asymmetrical pelvic attachment), which makes me wonder if it is the incidence or the diagnosis that is on the rise. A malformation of vertebrae, usually the last lumbar or first sacral vertebra (sometimes more than one per case) is simply and aptly called “Transitional Vertebrae”. This congenital and inherited defect begins in that stage of embryo development when differentiation is nearly complete, but a vertebral body “can not make up its mind whether it wants to be part of the lower lumbar vertebral column or part of the sacrum”, as colorfully described by OFA’s Dr. Greg Keller, and it winds up taking on bony characteristics of both lumbar vertebrae and sacrum. Less common are the transitional vertebrae seen at the thoraco-lumbar junctions. Wherever it is found, the affected part is called TVS, Transitional Vertebral Segment.
Veterinary-science observer Barbara Nibling describes mild cases
this way: “The processes are just a bit odd, one set of processes
looking as if the T13 (the 13th thoracic vertebral segment) belongs
to the lumbar group, while the other side looks like a normal T13.”
Many go unnoticed unless there is a rib on one side but not on the
other, in which case the difference leaps out at you. The affected
part is called TVS, Transitional Vertebral Segment. It apparently
can happen anywhere along the spinal column, but in the lumbo-sacral
area most often. If it results in less symmetry there, the condition
is usually referred to as “APA” — asymmetrical pelvic attachment.
The
transitional vertebral body takes on some of the characteristics of
both, and is an abnormality that may have a causative role in the
severity or nature of HD although, by itself, it seems not to have
any bad effects. Its developmental and inherited nature is extremely
probable, having been identified as familial and being similar in
many ways to other known genetic defects. Frequency of transitional
vertebrae runs from quite low (zero in Saints, 3% in Labs) to
somewhat higher (8-11% in German Shepherd Dogs), and most cases
(69%) are associated with HD. That is, most but not all cases are
found in dysplastic dogs. This is one reason why the frequency of
asymmetrical HD is as high as it is (30% in the GSD, for example —
more than in other breeds).
The
trait is probably polygenic; at least it cannot be said to be
simple. It is definitely familial. For example, Borzoi breeder
Bonnie Dalzell reports around 40% of the dogs that were radiographed
in a program she participated in had lumbo-sacral transitional
vertebrae! She described them as “much slower gallopers at field
trials than the dogs with normal anatomy” or having reduced interest
in running at a fast gallop. Top racers, she said, can go 33 mph,
while dogs with “weird backs” generally top out at 23 to 24 mph. She
also surmised that many cases might be missed, if the transitional
vertebrae were further toward the front of the dog, because of the
great size of her breed — the crest of the ilium of the pelvis and
the last lumbar vertebrae might not be included in the standard
17-inch film, and thus any TVS not observed. Field trial
performance, for which she is well known and highly respected, is
affected, so she naturally pays more attention to searching for the
anomaly than most people might. She has had eager coursing dogs with
TVS, and found them not as fast as the ones without it. Her
meticulous observation has uncovered other little-known “symmetry
anomalies” such as one in which there is an extra lumbar vertebra.
This would be highly unusual in dogs, although there is a breed of
pigs with an extra pair of ribs, and differences in number of
cervical vertebrae between animals such as giraffes and squirrels
(the numbers may surprise you!). Dogs with the extra vertebrae in
the loin and other lumbo-sacral anomalies seem to be prone to having
symptoms of something that vaguely resembles “Wobblers”, also
displayed neurological deficiencies in the hind legs, and were
relatively poor gallopers, according to Dalzell. Another fairly
location of transitional vertebrae is in the thoraco-lumbar region,
in which, she says, “the dog may have one less rib on one side than
the other. This does not seem to affect performance at a gallop.”
The
abnormal attachment of these segments causes the pelvis to be
rotated a little in a longitudinal fashion, which means the pelvis
is tilted so one femoral head gets more coverage by the acetabulum
than the other side does, and this tends to draw laxity or joint
ligament weakness into subluxation. Yet it is not so much the fact
that transitional vertebrae are there, as what effect they have on
pelvic attachment that is important. TVS does not participate in
causing HD unless it does so through intermediately causing APA.
Asymmetry in pelvic attachment is highest in Labs and GSDs (around
7-8%) and 79% of these cases are associated with HD. While
transitional vertebrae and asymmetrical pelvic attachment may not
cause all cases of unilateral HD, they do appear to uncover it or
make bilateral laxity look like unilateral HD, at least on the
hip-extended view. An important conclusion of this ten-year study is
that the quality of hip joints is not independent of the nature of
pelvic vertebral attachment.
The L7
to S1 region of the spinal column is where some see what they call
“block vertebra”, referring to a somewhat unusual shape. Not only
are affected coursing sighthounds slower, according to some in the
sport, but most dogs upon very careful motion analysis will evidence
an asymmetric gait. The last lumbar vertebra can be fused on one
side to either the first sacral vertebra, or its process (“wing”)
can bridge over to near the top of the ilium. In any case, the dog
has more articulation, and range of movement and flexion/extension
on one side than the other. Many have noticeably shorter stride, but
this can also be the result of other problems, such as arthroses in
any of the four limbs’ joints.
More
acronyms are not what I enjoy, but these abbreviations are helpful.
In orthopedic lingo, the condition of asymmetrical (without
symmetry) pelvic attachment of the last vertebrae before the sacrum
is called APA. The condition of transitional vertebral segments is
referred to as TVS. The fact that TVS and APA are associated with
unilateral HD or differences in the severity of one side vs. the
other, is why the OFA looks for these signs and requires a full
picture of the pelvis be included on each hip radiograph submitted
for evaluation/certification. The incidences of both APA and TVS in
“normal” dogs are quite low, but these conditions do exist
independently of HD in a small number of dogs with otherwise normal
hips. For example, APA was 2.8% and TVS 1.4% in Labrador Retrievers
with normal hip joints, but 13.8% and 5.2%, respectively, in
dysplastic Labs. There are similar or perhaps identical conditions
in humans. In people, TVS is an indicator of probable future
problems in the lower back.
Is it
a serious problem? Many think not, but I believe their lack of
concern is based on old information that indicated TVS was not a
significant problem. In a conversation between the OFA and GSD
fancier Rita Ledda (via e-mail chat list) about transitional
vertebrae, she was told that it is not a big problem; yet OFA
recommends an affected dog not be bred to a mate that also has
transitional vertebrae. They say that normally, TVS or APA by itself
(without concurrent HD or another disorder) does not affect the dog.
There might be some concern about dogs that engage in some type of
pulling competition, a popular sport in Malamutes, American
Bulldogs, and American Pit Bull Terriers. The stress may cause
irritation at the sacrum joint. It must be kept in mind that there
could be a relationship between TVS and other disorders, too. Morgan
et al found that in German Shepherd Dogs, at least, the presence of
lumbosacral transitional vertebrae is a predisposing cause of cauda
equina syndrome; this disorder will be treated below. Another GSD fancier, trainer, and writer named Ricardo Carbajal reported (on an e-mail list) a December 1996 conversation with OFA in which Dr. Keller said that TVS is a developmental problem. When the puppy is developing in utero, some of the lumbar vertebrae attach firmly or tenuously to the sacrum. You usually see bony changes that are more similar to the sacral area; one of those changes is that the transverse process (the side wing) deforms or “bends” and fully or partially fuses to the ilium. Some times you also see that the inter-vertebral space is diminished or absent. Usually this problem does not affect the health of the individual. But it does tend to run in families, so it should be considered a genetic defect and given whatever amount of serious attention you decide it deserves.
Morgan
has done much work in this area, and says that transitional
vertebrae “can occur at the site of junction of the major portions
of the vertebral column, i.e., occipito-atlanto-axial, cervico-thoracic,
thoraco-lumbar, and lumbosacral. The spinal segments at these sites
are altered so they have features in common with those either
cranial or caudal” [to them]. When we speak of transitional
vertebrae, we should also describe the specific nature of the
change, such as where the attachment is directed, and whether it is
unilateral or bilateral. Some TV are symmetrical, equal on both
sides. Others are asymmetrical (APA); “for example, a lumbar
transverse process on one side and a heavy wing on the other that
attaches to the sacrum.” Transitional lumbo-sacral vertebra (TLSV)
was found in 38% of German Shepherd Dogs diagnosed with cauda equina
syndrome. Is there a biochemical or genetic connection, or are such
dogs selected for by sloppy breeding practices in general?
For a
long time, it was generally thought that these abnormal vertebral
segments and attachments did not cause pain and therefore had little
clinical or breeding significance throughout a dog’s lifetime.
Currently, the feeling is that such lesions at the lumbosacral
junction predispose the dog to further weakness, instability,
excessive motion around that disc, creation of cauda equina
syndrome, and possibly a worsening of (already-present, even if
covert) hip joint laxity or instability. TVS can weaken an already
unstable sacro-iliac joint and put additional stress on the joint
between the sacrum and the last lumbar vertebra.
CES: CAUDAL EQUINA SYNDROME Description, Causes, and Symptoms
At the
caudal (rearmost) end of the spinal cord in the sacral and coccygeal
(tail) area, there are roots of several nerves named for their
resemblance to a horse’s tail. They emanate from the vertebral
column and branch out to various parts of the hindquarters. These
include the seventh lumbar nerve, the first three sacral nerves, and
the first five caudal nerves. The cord itself terminates around the
sixth lumbar vertebra in most dogs (Dachshunds are a bit different,
with the termination being one or two vertebrae distant). Some CES
is actually secondary and due to environment such as lumbosacral
disc degeneration. Sometimes people refer to the major manifestation
of the syndrome as Degenerative Lumbosacral Stenosis, as it
generally involves a compression of the nerve roots in the lower
back, at or near the junction of the sacrum with the last lumbar
vertebra.
Beyond
the sacrum, the vertebral bodies of the tail extend further than the
main cord does. If any of the vertebrae from L5 back toward the
tail are diseased, it can result in canine CES, which typically
involves some compression, destruction, or displacement of the nerve
roots which form the cauda equina. CES is called a syndrome instead
of a single traditional disease because there is no sole cause or
malady. When you have a number of disorders that have similar signs
and location they are lumped together (in both common and medical
parlance) as a syndrome. And of course, that means there can be a
number of different causes for this set of disorders. Thus, while
there may be various causes for the collection of symptoms, we see
similar reactions — namely, the filling in or stenosis (narrowing)
of either the cord canal or other “holes” through which pass veins,
arteries, and nerves. Just as a stenosis of the vertebral canal
further toward the head can produce Wobbler syndrome and other
disorders described in my book, compression of the cord in the
lumbosacral region or of these post-cord nerves as they exit from
between the last vertebrae of the spinal column before the last
three quarters of the tail can give both sensory and motor (feeling
and moving) nerve dysfunction. Even the blood vessels can be
compressed and fail to deliver nutrients or remove waste efficiently
from the rear limbs below. The impingement can take place in the
vertebral canal, or where the nerves exit the cord through the dura
mater (the fibrous covering of the cord), or between there and where
a nerve exits the canal between two adjacent vertebrae. If so, it is
probably caused by bone and cartilage changes in vertebral end
plates where the discs are attached.
Wherever they are pinched, the nerves, arteries, and veins lose part
of their functions and produce clinical signs. Most specialists
restrict the term cauda equina to symptoms arising from lumbo-sacral
area defects.
Congenital causes include spondylolisthesis
(slipping of one vertebra over an adjacent one somewhat similar to
Wobbler syndrome), malformations of the vertebrae, spina bifida,
perhaps spondylosis deformans, and stenosis of unknown origin. Cauda
equina syndrome can also be the result of acquired conditions such
as cancers, infections, disc disease or prolapse/protrusion, and
others. Cauda equina syndrome (entrapment and pressure on the nerve
root) can also be the result of arthritis or acquired conditions
such as cancers, infections, disc disease or prolapse, and others.
Some dogs will have more than one of these conditions at once.
Osteoarthritis can make CES worse or it can produce signs similar to
the syndrome by itself. Exercise can bring on the signs because
blood vessels dilate when one exercises, and dilated vessels can
press on the nerve roots; conversely, rest or tranquilizers may help
calm the dog and avoid pain until the condition improves, if it does
at all. Some CES cases involve a bone fragment from the sacrum that
detaches and moves into the spinal canal to press against the cord;
some call this “osteochondrosis of the sacrum”. In many of these,
there is an appearance of misalignment similar to what we see in
“Wobblers”. Many of these dogs have multiple spinal abnormalities,
which may be related to CES symptoms. Some have a persistent disk in
the sacrum, which means that the sacral segments did not fuse, as
they normally would have.
Many
also have transitional vertebral segment (TVS), but given that the
GSD breed is represented by so many of these cases, this may
possibly be somewhat coincidental. It also may be that research
facilities just see more GSDs than other breeds. Breed incidence
varies, but the GSD, at least in America, apparently does have a
higher incidence of spinal column disorders in the lumbo-sacral area
than do other breeds. Dr. Joe Morgan at Davis told me that his study
showed that dogs with cauda equina syndrome more often than expected
also have lumbo-sacral transitional vertebral segments (TVS or APA),
and that this combination was seen in the GSD more than in dogs in
general. Most affected dogs tend to be members of large, “athletic”
breeds.
As you
may have suspected, age is a factor in CES, with middle aged or
older dogs being more often afflicted. This causes a dilemma
regarding decisions to operate or euthanize or just wait to see how
long the dog can put up with the disease. Surgery seems to give
benefit for no more than two years in most cases. One of my
correspondents had a 14˝-year Boxer that was “going downhill”
rapidly, was on Rimadyl™ for a couple of months, and
enthusiastically dragged herself to the cookie jar for a treat. With
a bright mind, such a dog makes it very difficult for the owner to
decide. This Boxer was not “showing” any pain, according to the
owner. It also had a concurrent case of severe spondylosis, and was
certainly not the only such case of Boxers with both ventral
spondylosis and dorsal bony overgrowth/stenosis. Although most CES
cases are in older dogs, I have a friend in New Mexico who lost a
14-month old German Shepherd Dog puppy to the disorder. Diagnosis
To
accurately diagnose, expert radiography is highly recommended,
almost essential, but is only part of the whole work-up. Diagnosis
can be difficult, and may involve many ways of looking at the
problem: clinical signs (symptoms), neurological signs, radiography,
surgery, and deductive reasoning. In an early stage or in a more
sensitive dog, the only symptom might be progressive, sharp pain.
However, this pain or discomfort can show in a number of ways.
Intermittent lameness in one or both hind limbs or a stilted gait
like that of a Chow-Chow, more and more difficulty in rising to a
standing position, reluctance to jump, and perhaps sudden but
temporary lameness immediately after doing either of those things.
Strenuous activity may exacerbate these signs, just as it does in
hip-dysplastic dogs. The dog may express pain by as little as a moan
or whimper, or as much as a yelp or howl when moving or being
touched on the croup. As the Southern California Veterinary Referral
Group has stated, many dogs “are very tolerant of discomfort until
it eventually overrides their character and results in clinical
manifestations”. Sooner or later, even a Pit Bull Terrier or
Rottweiler (noted for being stoic) will indicate the burning sciatic
pain of the syndrome’s nerve root entrapment. Bowel and bladder
incontinence is common in advanced cases. Paresis or full paralysis
may occur.
As you
see, symptoms are many, with some resembling those of “Wobbler
syndrome”, some being mistaken for signs of HD. Its clinical signs
may also resemble degenerative myelopathy, axonal neuropathy, disc
protrusion, and tumors of the spine. It reportedly has its highest
incidence in GSDs and those breeds with high incidences of hip
dysplasia — which might not have any inherent connection. Not all
dogs with cauda equina syndrome have all the same symptoms, but
these may include straining with defecation, partial paralysis,
fecal or urinary incontinence, lameness, bunny hopping, and standing
with a hind leg drawn up. Leg pain is probably very similar to what
we humans call sciatica, judging from the identical locations of the
pinched nerves. Some probably have what humans refer to as a
“falling asleep” of the legs. This tingling may be a reason why some
dogs inflict damage to their tails and rear paws, in the form of
chewing, lick granulomas and other dermatoses. A similar thing
happens to many dogs with DM, but without pain.
Some
may show relatively early signs with a “dead” tail carriage. From SV
judge and then-chief-Körmeister Leonhard Schweikert regarding the
bitches at the huge GSD Sieger Show in Bremen, 2000 we have this
comment: “With respect to the evaluation of the rear, I noticed in
more than one case a lifeless or nearly lifeless tail. This is a
very worrisome fact, as this is one of the first indications of a
cauda equina syndrome (CES). We must look into this topic in the
near future in more depth.”
Neurologic examination usually begins with gait analysis.
Then the dog is tested for pain and neurologic dysfunction to
confirm the suspected site of the lesion. Physical exam of the
standing dog reveals an exaggerated response to the pain of
extending the hip joint, which in turn extends the lumbosacral
joint. This is very subjective; dogs with moderate to severe HD will
often show a mild response to hip extension, but dogs with
lumbosacral disease such as CES will often complain more when the
vet extends the hip and presses on the croup (lumbosacral junction).
This can also be seen if the dog attempts to “stretch” or straighten
(extend) its back, because part of the disc and a ligament are
pushed into the spinal canal space occupied by the nerves.
Manipulating and lifting the tail typically elicits an exquisite
pain response. Pain is also caused by deeply palpating the muscles
over the croup and loin. Spinal reflexes such as the perineal reflex
(beneath anus and vulva or scrotum) and anal tone are tested.
Diagnosis is sometimes much a matter of differentially
distinguishing this syndrome, i.e., ruling out other disorders by a
process of elimination. Since cauda equina syndrome affects mostly
German Shepherds, the vet is challenged to decide whether the
symptoms are those of GSD myelopathy instead, which he can do by
determining whether there is pain and where the motor neurons are
affected, high or low.
Ordinary radiographs are not very useful in diagnosing syndromes
such as CES and distinguishing it from (or ruling out association
with) infection, trauma, severe arthritis or bone cancer. Special
x-ray procedures may be required for a definitive diagnosis.
Myelograms and/or epidurograms (contrast dye studies of the spinal
canal) can help to confirm the location of the lesion and the
position of any ruptured disc in relation to entrapped nerve roots
as the spine is flexed and extended. The Southern California
Veterinary Referral Group that I mentioned earlier says, “With new
gas anesthetics, advanced monitoring equipment, and modern contrast
agents for the dye study, the myelogram and epidurogram are now
common and safe diagnostic procedures when performed under the
proper conditions. In difficult cases, MRI or CT scans are available
and are of exceptional diagnostic value. Electromyography (EMG) may
be of value in substantiating the diagnosis and the severity and
symmetry of nerve root entrapment.” I know that in the many cases of
human disk disease that I have had opportunity to ask about because
of a possibility of back surgery for myself, the epidural is
extremely uncomfortable (people are generally not knocked out for
the insertion of the needle into the nerve!) and if used for pain
relief, is only temporary; if used to inject dye, it is not only
painful for an extended time, but also is reportedly risky. MRI or
CT is very expensive, and very few vets have the equipment.
One
Morgan et al study divided hundreds of study dogs into 3
groups segregated by whether or not the dogs had diagnosed
degenerative disc disease (DDD) involving lumbosacral discs and
transitional vertebral segments (TVS), and whether the dog had CES.
Their data suggested an association between TVS and CES and an
association between DDD and CES: more CES when DDD and TVS were both
evident. Some CES seems to be partially dependent on the presence of
TVS. They also say that TVS is probably an inherited condition.
Morgan believes that GSDs have a higher frequency of TVS than other
breeds do, and that may partially explain the higher incidence of
CES in GSDs. TVS therefore should be part of the criteria in
selection of breeding stock. The study size is small, but a warning
sign nevertheless. Treatment of Cauda Equina Rest and anti-inflammatory/analgesic medications are often prescribed for the first episode, when mild pain only is experienced, and when patient age or client’s monetary situation indicates that to be the best course. Treatment with medications such as analgesics, steroids, chloramphenicol, tranquilizers, and sedatives have temporary effect at best; surgery has variable prognosis depending on the cause(s) of the syndrome. Neurologic signs, continued, frequently recurring, or considerable pain that does not respond to conservative treatment, call for surgical treatment. To relieve pressure on the entrapped roots, a dorsal laminectomy is one of the choices. Removal of parts of the vertebrae or fusion of two vertebrae together are some of the procedures chosen. In some cases, the vertebral segment is sliced horizontally, the top lifted, and extra space thereby created. If this is done on only one side, it is called a hemi-laminectomy. Unfortunately, scar tissue can make the situation as bad or worse in a year or more afterwards; thickening of ligaments or cartilage may be part of the body’s way of trying to compensate and stabilize. But in general, surgery is far preferable to medication. Exposing the nerve roots in a more-or-less conservative surgical approach allows one to safely retract them and expose the disc space. “The cauda equina is gently retracted to one side with blunt nerve hooks, exposing the herniated discs as a large dome on the floor of the spinal canal. The herniated disc is excised, compressive osteophytes removed, and foramenotomies (opening the nerve root canals) performed to relieve root entrapment. Once the pressure is relieved, the neurologic function gradually returns as the nervous tissue heals in its decompressed environment.”
Considering treatment? Shop around. Don’t spend too much money. Use
common sense in spending your common cents. Postoperative Care
Rest
for at least 6 weeks is recommended post-surgery. That means, cut
out the strenuous activity. Short walks on leash at first, then
gradually increase the amount of exercise. Keep the dog lean and
fit; obesity exacerbates most diseases and prolongs recuperation.
Prognosis depends on severity of signs before surgery. Dogs with
chronic neurologic dysfunction may never recover to a satisfying
lifestyle, but at least they will enjoy a pain-free life. Similar Signs and Conditions
One
consulting client described her dog thus: “Her back is hunched, she
wobbles and she acts as if she has HD but her x-ray showed that her
hips are normal.” I told her that she should ask her vet to
investigate the possibilities of spondylosis, TVS, and CES.
Spondylosis deformans is a condition in which bridges are formed
along the ventral (bottom) parts of the vertebrae, starting with the
last lumbar segment and, with time, extending to progressively more
forward segments. There is no spinal cord compression in this
disorder, but pain may come from encirclement or pressure on nerve
roots leading out from the cord to peripheral nerves. Differential
diagnosis should rule out discomfort from concurrent arthritis,
cauda equina syndrome, or other problems. If one of these bony
bridges breaks, there could be considerable pain and inflammation in
the surrounding soft tissues.
Transitional Vertebral Segment, TVS, has quite a few of the same
symptoms as spondylosis and CES, but they are more subtle; in fact,
TVS is highly unlikely to give any signs at all. Only when
accompanied by HD or the dog is routinely radiographed for a pelvic
picture do people generally know that their dogs have it. However,
remember that Morgan found that in German Shepherd Dogs, at least,
the presence of lumbosacral transitional vertebrae seems to be a
predisposing cause of cauda equina syndrome. He says that
transitional vertebrae can occur at the lumbosacral portion of the
vertebral column. Some TV are symmetrical, others are asymmetrical
pelvic attachments (APA); “for example”, he says, “a lumbar
transverse process on one side and a heavy wing on the other that
attaches to the sacrum.” TVS can weaken an already unstable sacro-iliac
joint and put additional stress on the joint between the sacrum and
the last lumbar vertebra.
Congenital spinal stenosis,
according to Morgan, is a primary narrowing of the canal with
resultant compression of the cord. It’s like it is strangling it and
preventing proper transmission of the electrochemical neural
impulses. He says such a constriction is a cause of CES when it
involves the last lumbar or the first couple of sacral vertebral
segments. However, it may be seen without the typical symptoms of
CES. The word primary in this context means a disorder that has no
apparent origin in a different disorder; i.e., it is not secondary
to another disease state or syndrome. Primary stenosis is possible
anywhere, but is more often seen at the area where cervical and
thoracic vertebrae meet, and at the lumbosacral junction. Bone
tissue looks normal except the shape of the segment is different,
with shortened parts and narrower canal space.
While
I have tried to present most of the disorders in bones and joints in
my book on orthopedic disorders, it must be remembered that there
are many less known and infrequently encountered. In the case of the
spinal column, for example, there are also such aberrations as
failure of sacral vertebrae to fuse, sometimes referred to as
lumbarization of the first sacral segment. This can be considered as
a variant of TVS, though slightly different than what we are used
to.
Osteochondrosis of the sacrum is found on the cranial end plate of
the sacrum, on the lumbar side, is similar in appearance to
osteochondrosis in joints, and superficially resembles avulsion
fractures. Breeding
Is it
wise to use a CES dog in breeding? Unless there is associated HD and
osteoarthritis starting to be evident in the hip joint (rim, femoral
neck, pectineal eminences, etc.), or there are several in your dog’s
family that have the syndrome, or the signs are severe enough to
cause real discomfort and interfere with breeding, some people tell
us not to worry about it. They say that you can look instead to
whether the dog has enough other qualities to keep him in the gene
pool. I believed that for a while, but then when I saw the increase
in number of cases reported, I decided we should not be that
complacent. Kitty Porter of Duke University had a CES dog, and
preferred to think of TVS as not “pathological” (by which she meant
serious and inherited). Perhaps we need to reevaluate our
preferences from time to time. CES might not be the worst problem in your breed, but still, it is not wise to perpetuate the sort of weakness that allows defects such as CES to be perpetuated, however minor the ailment may seem at first. There are enough dogs that have had to be euthanized for us to take this disorder seriously and assume genetic components to exist. Transitional lumbo-sacral vertebra (TLSV) was found in 38% of German Shepherd Dogs diagnosed with cauda equina syndrome. Is there a biochemical-genetic connection, or are such dogs selected for by sloppy breeding practices in general? For a long time, it was generally thought that these abnormal vertebral segments and attachments did not cause pain and therefore had little clinical or breeding significance throughout a dog’s lifetime. Currently, the feeling is that such lesions at the lumbosacral junction predispose the dog to further weakness, instability, excessive motion around that disc, creation of cauda equina syndrome, and possibly a worsening of hip joint laxity or instability. ******************************************************** SPONDYLOSIS DEFORMANSby Fred Lanting
Spondylosis deformans is a condition in which bridges are formed
along the ventral (bottom) parts of the vertebrae. It has been
diagnosed in man, domestic cats (68%, yet no symptoms!), bulls, and
even whales as well as in dogs. It is suspected that bulls on
high-calcium diets may have increased susceptibility. The term
“spondylitis” literally means “an inflammation of the spine”,
especially the bone, and spondylosis is sometimes used as a synonym
as well as for describing types of ankylosis. One of these types is
a bone proliferation, usually on the ventral surfaces of adjacent
vertebrae, producing a bridge from one to the other. This condition
is best known as spondylosis deformans. There is no spinal cord
compression, but the spine is immobilized in that location. If the
condition continues to spread, there may be several such bridges,
“welding” a series of vertebrae into an inflexible backbone. It is
seen fairly easily via lateral radiography. Because of different
degrees seen in different breeds, I believe there to be more than
one genetic determinant for this disorder, though nutrition may play
a modifying role. I know full well the familial line in a
significant portion of American German Shepherd Dogs with this
problem, but there are some “German” lines with it, too. As in
Wobbler Syndrome, much growth of osteophytes can occur, and
encirclement or pressure on nerve roots leading out from the cord to
peripheral nerves may be part of the reason some dogs have been
reported to show a little pain, but generally the animal does not
appear to be suffering and such discomfort more likely comes from
concurrent arthritis, cauda equina syndrome, or other problems.
Males seem more at risk than females.
It is
not completely clear how this disorder progresses, but it may start
with a breakdown of Sharpey’s fibers, which are the fibers making up
the annulus or outer portion of the intervertebral disks.
Subsequently, inner disk material protrudes, stretching the
longitudinal ligament, and promoting the appearance of osteophytes
which grow out from the vertebral bodies in such a way that one
cannot tell where the original bone ends and the osteophytic growth
begins. Before that happens, though, separate ossification centers
can be seen forming a few millimeters from the vertebral bodies;
they later fuse and grow toward the adjacent vertebral segment.
Eventually, and depending on breed and family history, the disk
spaces between particular segments are bridged. True ankylosis
(complete fusion into a continuous bony bridge between vertebrae) is
far less common than the near-junction of these osteophytes, and is
much more likely on the last lumbar segments. Very seldom do the
osteophytes grow upward or in such a way as to pinch the spinal cord
or otherwise cause neurological signs, so spondylosis deformans
might be considered a relatively benign disorder when compared with
HD, elbow dysplasias, wobbler syndrome, etc.
All
the dogs I have known with ventral spondylosis have gradually become
inflexible in the spinal column, and required ramps instead of
stairs, for example. But pain is not a usual part of the spondylosis
pathology, unless the bridges fracture, which is highly uncommon.
Many affected dogs live satisfactory lives, though somewhat limited
in flexibility and range of motion. Fortunately, by the time
spondylosis deformans becomes noticeable in clinical signs, the dog
may be considered “retired” from his duties of running around,
jumping, and doing the other things expected of a youngster. In some
individuals, it will get worse suddenly rather than continue in a
gradual worsening. Possibly, trauma may bring fracture of the bridge
created in the development of spondylosis, which crack may spread to
the arch and body, thus pinching the cord.
Often, spondylosis will be discovered on radiographs
incidentally while the vet is looking for something else, such as a
cause for lameness. In some of these cases, he may be tempted to
make his diagnosis right then, and not to look further for the
actual main cause, which may include HD, osteochondrosis in other
joints, tumors, and others. Osteoarthritis of the spine
(inflammation of the joints between vertebrae) is not the same
disorder, nor is true spondylitis (an inflammation of the vertebrae
themselves, brought on by either trauma or infection). Remember that
“-itis” means inflammation, and spondylosis deformans in itself is a
non-inflammatory degenerative disease.
Owners and their veterinarians should distinguish
between what I call “classical” spondylosis and a somewhat different
form. In a Mastiff breeders’ 2003 Internet chat group, Canadian vet
Dr. Claire Duder says, “Not all spondylosis is created equal. Most
dogs with spondylosis will have radiographic lesions on one or a few
intervertebral joints, and in the majority of cases, the dogs will
act perfectly normal. On the other hand, some dogs with spondylosis
of the lumbo-sacral joint (where the spine and the pelvis meet) can
experience severe pain. This latter subset of dogs may well benefit
from surgery. Surgical treatment for L-S spondylosis should only be
considered for those dogs who demonstrate narrowing of the spinal
canal (actually, the spine ends a bit above this area, but there are
still lots of large spinal nerves going through) via myelogram or
MRI. Sometimes this narrowing is only present radiographically in
certain positions. Surgery is designed to reduce pressure on the
spinal nerves, and is usually done in specialty centers only.”
She
was talking about surgery for lumbo-sacral disease only. She told me
she had never referred a dog for surgical repair of spondylosis
anywhere except at the L-S joint — and that it does not seem to be
common practice even there. If a myelogram or an MRI showed
narrowing of the spinal canal or foramina, she supposed it would be
an option. As in CES, the surgical approach is dorsal (going in from
the back instead of via the abdominal cavity), and the objective is
to reduce pressure on the spinal nerves by removing all or some of
the “roof” of bone over the affected area. The technique of cutting
and removing part of that bony roof, often including the spinous
process that juts upward like the mast or chimney of a ship, is
called a dorsal laminectomy (hemi-laminectomy, if you only do one
side).
Lumbo-sacral spondylosis is much more likely to be
clinically significant than spondylosis in other areas of the spine;
i.e., more likely to involve pain and influence movement. One
deciding issue regarding surgery is whether the nerves are being
compressed by structural changes of the L-S joint. As Dr. Duder
says, “The bony overgrowths seen on radiographs are usually not the
cause of the problem, but are themselves a symptom of, and a
response to, the underlying instability of the articulation. It
matters not if there is a big hunk of bone on the ventral surface of
the joint, as long as the dorso-lateral surfaces, where the nerves
exit, and the spinal canal are unaffected.” I agree, and have
counseled friends to get a second opinion when surgery has been
discussed. There really is no operation that has a high confidence
rating or good prognosis for classical ventral spondylosis. It is
probably better to keep the dog comfortable until euthanasia is
needed, providing you have obtained a good diagnosis, and other
disorders have been ruled irrelevant or absent. Analgesics are
frequently prescribed (vets and M.D.s like to push pain medication
almost as frequently and enthusiastically as they do antibiotics and
steroids) but I have yet to see any reason or excuse for their use
for typical spondylosis, backed up by a scientific study. Rimadyl,
Deramaxx, and other analgesics might be somewhat effective initially
in relieving symptoms of CES and dorsal lumbo-sacral disease, but
not indicated for ventral spondylosis. I would not put much
currency (defined both ways!) in any vet’s prescription for
painkillers if he did not find hard evidence of pain, or something
other than the ventral vertebral bridging of classical spondylosis
on the radiographs!
An intervertebral inflammation resulting in fusion
of the vertebrae has been seen in humans and is known as ankylosing
spondylitis. It is related to both adult and juvenile rheumatoid
arthritis, and the similarity to spondylosis deformans in the dog
(minus the inflammation) once made me wonder if there is a common or
similar genetic defect in the “immune systems” of man and beast.
Although it has been misnamed ankylosing spondylitis in the past,
spondylosis deformans in the canine is not that disorder, exactly.
Senile ankylosing hyperostosis is a syndrome in humans that is
considered to be a variation of osteoarthritis characterized by
large osteophytes, also shows bridging between and on the
anterolateral (front and side) surfaces of the vertebral bodies. In
man, it appears mainly in males over 50 years of age, giving
symptoms of minor to moderate back pain, stiffness, and lack of
flexibility. Bone spurs and ossification in tendons and ligaments
are common. Even intervertebral osteochondrosis may be a separate
disorder; although also a result of disk degeneration, it is
characterized by reduced disk height and vertebral end-plate
sclerosis, not seen in spondylosis deformans.
The genetic transmission of the tendency to develop
spondylosis deformans is obvious to anyone who has watched it appear
in offspring of certain dogs, generation after generation. But
exactly how (the etiology) is not as sure. Perhaps there is an
inherited weakness in how a dog’s vertebrae respond to or withstand
repeated microtraumas; perhaps in some lines, the blood vessels that
serve the outer layers of the disks regress and disappear faster
than the normal or expected three or four years. It seems to be a
fairly natural consequence of aging, as 75% of dogs in some breeds
are affected to some degree by 9 years, and half by 6 years. On the
other hand, some work has indicated that spondylosis deformans is
more a disease of middle age. Breed and family variables make the
incidence figures vary tremendously. It became a very noticeable
disorder in the German Shepherd Dog when, for a while, 90% of the
“show” GSDs in the USA were allegedly descended from one very
popular late-1960s American Grand Victor (twice) who had and passed
along this disease in a severe form (estimate based on a pedigree
study reported in a GSD magazine several years ago). Great Danes are probably the most likely to develop this disorder, followed by mastino/mastiff types that are historically related. Boxers also appear to be at relatively high risk for spondylosis. Among the many that have corresponded with me was the owner in northern Michigan who reported a few things with her 6-year-old male that are not typical: panting, emaciation, and vomiting, in addition to limping and refusal to run. The vet “discovered his spine was fusing together and new bone was being formed over the top” and mentioned spondylosis. Unfortunately, this is like steering a car in two directions at once, since we think of spondylosis as bone proliferation on the bottom (ventral) surfaces of the vertebral segments, not the top. I suggested she also have the vets look for possible tumors/cancer on the spinal cord or associated tissues, heartworm, kidney failure, liver function insufficiency, CES, and Addison’s Disease as potential causes for the other symptoms. Rimadyl had been administered, and the owner thought there might have been some temporary help. Another vet prescribed Deramaxx without even looking at the radiographs! This Boxer owner previously had his dam, who “developed the same symptoms when she was nearly nine. She could barely walk at the end and threw up frequently. The vet we had at the time didn’t know what she had, although her white blood count was high and her spine was fused too.” This is a strong indication that an inherited weakness should preclude such dogs from being bred.
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